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Cases of word blindness are always interesting, and this case is, I think, particularly so. It is unique, so far as I know, in that it follows upon no injury or illness, but is evidently congenital, and due most probably to defective development of that region of the brain, disease of which in adults produces practically the same symptoms—that is, the left angular gyrus.

I may add that the boy is bright and of average intelligence in conversation. His eyes are normal, there is no hemianopsia, and his eyesight is good. The schoolmaster who has taught him for some years says that he would be the smartest lad in the school if the instruction were entirely oral. (Morgan, 1896, p. 1378)

Hinshelwood, in turn, used Morgan’s case as an impetus to turn his attention to congenital, in addition to acquired, word-blindness. From the late 1890s into the early 20th century, Hinshelwood gathered data on several cases of acquired and congenital word-blindness and published his observations in his classic volume, Congenital Word-Blindness (Hinshelwood, 1917). He was one of the first to note at least two important aspects of reading disability in children. First, he noted the preponderance of males with the condition. Out of the 12 cases he presented in the book, 10 of them were males. Furthermore, he cited an article published in Lancet in 1904 by Stephenson, in which the author had commented that of the 16 cases reported up until then in the literature, 13 of them were males.

Second, Hinshelwood highlighted the potentially inherited aspect of reading disability. He reported on six cases within two generations of the same family:

If we analyze the symptoms manifested by these six cases, we are struck with their similarity. The symptoms of all six children were practically identical in kind, but only differed in degree. Their defect was strictly confined to their inability to recognize by sight, words and letters, with one exception, that of Case XI, where the inability was extended to numbers also. (Hinshelwood, 1917, p. 72)

Furthermore, he cited a growing body of literature published in several journals (e.g., Lancet, The Ophthalmoscope, Ophthalmic Review) of cases of congenital word-blindness occurring within close relatives. Similar to the literature on gender, the cases were relatively few in number; however, evidence was accumulating to suggest that congenital word-blindness was primarily manifested in males and was often inherited.

Hinshelwood also addressed the issue of diagnosis and prevalence of word-blindness, foretelling current- day debates over these issues:

In my first contribution on this subject I said: “I have little doubt that these cases of congenital word-blindness are by no means so rare as the absence of recorded cases would lead us to infer. Their rarity is, I think, accounted for by the fact that when they do occur they are not recognized.”

  • In educational circles there was even a tendency to exaggerate the frequency…and I find…the

statements “that these cases…are of very common occurrence,” and that “one in every thousand of the children in our elementary schools at least shows this defect.” …

The truth is that this great divergence of opinion…is simply due to the fact that some later writers have extended the term congenital word-blindness to include slight degrees of defect in the visual word center, while the earlier writers had reserved it only for those grave cases which could be regarded as pathological. (Hinshelwood, 1917, pp. 76–82)

Hinshelwood postulated that the primary disability these children had was in visual memory for words and letters. Thus, his educational recommendations, although not very specific, dealt with training children to increase their visual memory for words. Furthermore, he was a strong advocate for intensive, individualized one-on-one instruction: “It is not possible to teach such children in ordinary elementary schools…. The first condition of successful instruction in such cases…is that the child must have personal instruction and be taught alone” (Hinshelwood, 1917, p. 99).4

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